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Depending on the severity of the DNA damage, the cells may no longer be able to undergo repair and either go through apoptosis or cell senescence. [8] Such senescent cells in mammalian culture and tissues retain DSBs and DDR markers. [14] It has been proposed that retained DSBs are major drivers of the aging process. Mutations in genes relating ...
This ensures that the cell cannot enter the next stage of cell division unless the DNA damage is repaired. However, the p21 cells can trigger apoptosis. Apoptosis or programmed cell death is associated with gradual degradation of the immune system, skeletal muscle, and aging-associated malfunction. [32] Naked Mole Rat.
Senescence can be induced by several factors, including telomere shortening, [37] DNA damage [38] and stress. Since the immune system is programmed to seek out and eliminate senescent cells, [39] it might be that senescence is one way for the body to rid itself of cells damaged beyond repair. The links between cell senescence and aging are several:
Aplastic Anemia is often an adverse effect of certain medications [17] but as such it cannot really be considered as evidence against the stem cell theory of aging. The cellularity of the bone marrow does decrease with age and can be usually calculated by the formula 100-age, and this seems consistent with a stem cell theory of aging. [18]
Extending telomeres can allow cells to divide more and increase the risk of uncontrolled cell growth and cancer development. [24] A study conducted by Johns Hopkins University challenged the idea that long telomeres prevent aging. Rather than protecting cells from aging, long telomeres help cells with age-related mutations last longer. [13]
Senescent cells are highly metabolically active, producing large amounts of SASP, which is why senescent cells consisting of only 2% or 3% of tissue cells can be a major cause of aging-associated diseases. [32] SASP factors cause non-senescent cells to become senescent. [39] [40] [41] SASP factors induce insulin resistance. [42]
Senescence (/ s ɪ ˈ n ɛ s ə n s /) or biological aging is the gradual deterioration of functional characteristics in living organisms. Whole organism senescence involves an increase in death rates or a decrease in fecundity with increasing age, at least in the later part of an organism's life cycle.
The free radical theory of aging states that organisms age because cells accumulate free radical damage over time. [1] A free radical is any atom or molecule that has a single unpaired electron in an outer shell. [2] While a few free radicals such as melanin are not chemically reactive, most biologically relevant free radicals are highly ...